Q Chen A / Y Wang (@5.5) vs M Kawamura / F Kozaki (@1.12)
10-09-2019

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M Kawamura / F Kozaki will win
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Q Chen A / Y Wang – M Kawamura / F Kozaki Match Prediction | 10-09-2019 02:30

We aimed to effectively evaluate the strength of evidence from the available literature regarding the usefulness of dietary bioactives whilst, simultaneously demonstrating the features of the DIANA software and its ability to synergistically strengthen data from the literature. To conclude, dietary bioactives modulate miRNA which in turn have effects on cancer development and progression. Rather than seeking a needle in a haystack, we liken the use of DIANA software together with Tarbase, as dramatically reducing the size of the miRNA pool to be investigated, to something more manageable from a logistical and financial point of view. Such evidence sourced from experimentally supported interactions as seen in Tarbase v7.0, implies that we can be relatively confident, keeping the limitations in mind, that the information provided can be applied in the laboratory to investigate diet-miRNA interactions in the context of cancers.

Self-Assembled Three Dimensional Network Designs for Soft Electronics [pdf]K.-I. Li, H.U. Jang, K. Lee, B.H. Yang, A. Kim, J.-H. Lee, Y. Yu, B.J. Jeong, Y.M Song, Y. Kim, J. Jung, J. Song, C. Chung, S. Kim, H. Xu, H.N. Huang, Y. Jang, K.J. Kim, J.W. Lee, J.-W. Liu, J.Y. Yu, J. 46. Kwak, H.H. Zhang and J.A. Wang, Z. Yang, J.W. Jung, Y.

Yang, D.W. Lee, S. Ghaffariand J.A. Huang, R. Xu, Y.H. Ferromagnetic, Folded Electrode Composite as a Soft Interface to the Skin for Long-Term Electrophysiological Recording [pdf]K.-I. Liu, Y.J. Paik, Y.G. Kim, A. Kwak, Y.Y. 43. Song, J.H. Jang, H.N. Kim, B.H. Ma, J.-W. Feng, U. Jung, J.W. Banks, J.W. Jeong, Y.M. Shi, Z.J. Wei, X.

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Kim, C.F. Wang, L. Hu, C.H. Lei, N.H. Chen, T.J. Zhang, W.X. Li, Y.S. Ward, A. Li, H.J. Hao, Y. Nomoto, T.S. Pisano, Y. Huang, Y.F. Wang, A. Three-Dimensional Integrated Stretchable Electronics [pdf]Z.L. Pan, Y. Linand S. Durstock, A. Maralani, X.S. 51. Zhang, J.W. Li, M.F. Gu, Y.M.

Unfortunately little is known about miR-3935, although it has been found to be down-regulated in some neurodegenerative disorders 62, and up-regulated expression reduced proliferation and migration in A549 cells 23 . Interestingly, circulating levels of miR-29a have also been proposed as a biomarker for cancer progression in colorectal cancer 61. Similar to miR-221 and miR-222, miR-29a influences cell proliferation and the cell cycle by down-regulating p42.3, however, it acts as a tumour suppressor rather than an oncogene 60.

Li, B.H. Huang, U. Jang, Y.C. Wu, S. Kim, S. Banks, K.J. Soft, Thin-Skin Mounted Power Management Systems and Their Use in Wireless Thermography [pdf]J.W. Xu, S.Y. Jang, P. Kim, J.Y. Yu, J. Paik and J.A. Lee, K.-I. Choe, S. 41. Yang, A. Huh, Y.H. Lee, R.X. Ma, S.W. Won, Y.H. Kwon, Y.G.

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Li, S.H. Zhou, Y. Chen, Y.S. Sternini, Q.F. Lee, Z.L. Zhang, N.H. Teng, W.B. Zhou, M. 49.Stretchable Ultrasonic Transducer Arrays for Three-dimensional Imaging on Complex Surfaces [pdf]H.J. Guo, Y. Wang, L. Kim, Y.X. Wang, Y. Huang, R.M. Li, A. Gu, Y.M. Chen, Z.Y. Pharr, F. Zhu, C.H. Hu, X. Nomoto, S. Zhang, X.S. Lei, T.J. Chen, C.F. Lanza di Scalea and S.

Bioactives such as polyphenols and isoflavones found naturally in our food are increasingly being recognised as regulators of interest. We carried out a literature review wherein we assessed the impact of three dietary compounds, namely butyrate, genistein and quercetin, on miRNA expression followed by an in silico study utilising DIANA-miRPathv3 software. These compounds can regulate cancer pathways through microRNAs which are critical in modulating expression of various genes. Diet plays a major role in regulating cancer. The in silico analysis identified key pathways of interest such as bladder cancer which had significant interactions with the miRNAs modulated by the dietary compounds. Our literature search found that miR-34a, miR-200a-3p and miR-200b-3p were modulated by all three compounds while miR-221, miR-222, miR-29a, miR-3935 and miR-574-3p were modulated by both genistein and butyrate and let-7b, miR-194, miR-96-5p and miR-424 were modulated by butyrate and quercetin.

Xu, G. Azam, S. Tang, Y.-H. Yen, J. Wang, T.M. Lee, S.S. Liu and R. Lo, B.P. Wang, H.M. Array Atomic Force Microscope for Real-Time Multiparametric Analysis [pdf]Q.Q. McCulloch, S. John, Z.W. Ma, K.M. Cauwenberghs, A.D. Wang, N. Yang, Q. Herum, C.H. Patel, J. 55. Head, F.

Mio Kozaki vs Eunyeong Park Live Center

These two miRs are a part of the miR-200 family and have been shown to modulate cancer invasion by regulating epithelial to mesenchymal transition (i.e. This results in uncontrolled proliferation of cells 49, 50 which is a hallmark of cancer. As miR-34a regulates key pathways in cancer, it is important to note that its non-specific regulation serves as a readily available target for cancer treatment. Therefore, there is merit in regulating the miR-34a - p53 relationship as p53 inactivation via gene expression changes, is one of the most frequent alterations seen in human cancers 49. p53 tumour suppressor protein has long been recognised as a critical regulator of genes related to cell-cycle arrest (significant pathway of interaction as seen in Tables 2 and 4), apoptosis, increased DNA repair and/or inhibition of angiogenesis 51, 52. MiR-574-3p is reportedly a tumour suppressor miR, and it has been inversely associated with post-operative tumour relapse in patients treated for esophageal squamous cell carcinoma 56. Furthermore, genistein treatment led to miR-34a re-expression in AsPC-1 prostate cancer cells which contributed a 30% inhibition of cell proliferation and increased apoptosis 32. Genistein, butyrate and quercetin also modulated the expression of miR-200a-3p and miR-200b-3p. MiR-34a also presents a unique opportunity and need for further investigation due to its non-specific regulation. metastasis) 55. Other bioactives such as curcumin 53, resveratrol 11 and polyunsaturated fatty acids 54 were also shown to modulate the expression of miR-34a. This study shows the applicability of using genistein treatment in miR-34a expression and demonstrating the direct effects its modulation has on cancer cell growth. Reduced expression of miR-34a in cancer, results in abnormalities in the p53-apoptotic pathway.